Burkholderia pseudomallei |
|
B. pseudomallei colonies on Ashdown's agar showing the characteristic cornflower head morphology. |
Scientific classification |
Kingdom: |
Bacteria |
Phylum: |
Proteobacteria |
Class: |
Beta Proteobacteria |
Order: |
Burkholderiales |
Family: |
Burkholderiaceae |
Genus: |
Burkholderia |
Species: |
B. pseudomallei |
Binomial name |
Burkholderia pseudomallei
(Whitmore 1913)
Yabuuchi et al. 1993[1] |
Synonyms |
Bacillus pseudomallei Whitmore 1913
Bacterium whitmori Stanton and Fletcher 1921
Malleomyces pseudomallei Breed 1939
Loefflerella pseudomallei Brindle and Cowan 1951
Pfeiferella pseudomallei
Pseudomonas pseudomallei (Whitmore 1913) Haynes 1957
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Burkholderia pseudomallei (also known as Pseudomonas pseudomallei) is a Gram-negative, bipolar, aerobic, motile rod-shaped bacterium.[2] It infects humans and animals and causes the disease melioidosis. It is also capable of infecting plants.[3]
B. pseudomallei measures 2-5 μm in length and 0.4-0.8 μm in diameter and are capable of self-propulsion using flagellae. The bacteria can grow in a number of artificial nutrient environments, especially betaine- and arginine-containing.
in vitro, optimal proliferation temperature is reported around 40°C in pH-neutral or slightly acidic environments (pH 6.8–7.0). The majority of strains are capable of fermentation of sugars without gas formation (most importantly, glucose and galactose, older cultures are reported to also metabolize maltose and starch). Bacteria produce both exo- and endo-toxins. The role of the toxins identified in the process of melioidosis symptom development has not been fully elucidated.[4]
Contents
- 1 Identification
- 2 Disinfection
- 3 Medical importance
- 4 Antibiotic treatment and sensitivity testing
- 5 Pathogenicity mechanisms and virulence factors
- 6 Vaccine candidates
- 7 References
- 8 External links
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Identification
B. pseudomallei is not fastidious and will grow on a large variety of culture media (blood agar, MacConkey agar, EMB, etc.). Ashdown's medium (or Burkholderia cepacia medium) may be used for selective isolation.[5] Cultures typically become positive in 24 to 48 hours (this rapid growth rate differentiates the organism from B. mallei, which typically takes a minimum of 72 hours to grow). Colonies are wrinkled, have a metallic appearance, and possess an earthy odour. On Gram staining, the organism is a Gram-negative rod with a characteristic "safety pin" appearance (bipolar staining). On sensitivity testing, the organism appears highly resistant (it is innately resistant to a large number of antibiotics including colistin and gentamicin) and that again differentiates it from B. mallei, which is in contrast, exquisitely sensitive to a large number of antibiotics. For environmental specimens only, differentiation from the non-pathogenic B. thailandensis using an arabinose test is necessary (B. thailandensis is never isolated from clinical specimens).[6] The laboratory identification of B. pseudomallei has been described in the literature.[7]
The classic textbook description of B. pseudomallei in clinical samples is of an intracellular bipolar-staining Gram-negative rod, but this is of little value in identifying the organism from clinical samples.[7] It has been suggested by some[8] that the Wayson stain is useful for this purpose, but this has been shown not to be the case.[9]
Laboratory identification of B. pseudomallei can be difficult, especially in Western countries where B. pseudomallei is rarely seen. The large wrinkled colonies look like environmental contaminants and are therefore often discarded as being of no clinical significance. Colony morphology is very variable and a single strain may display up multiple colony types,[10][11] so inexperienced laboratory staff may mistakenly believe the growth is not pure. The organism grows more slowly than other bacteria that may be present in clinical specimens, and in specimens from non-sterile sites, is easily overgrown. Non-sterile specimens should therefore be cultured in selective media (e.g., Ashdown's[12][13] or B. cepacia medium.[5] Even when the isolate is recognised to be significant, commonly used identification systems may misidentify the organism as Chromobacterium violaceum or other non-fermenting gram-negative bacilli such as Burkholderia cepacia or Pseudomonas aeruginosa.[14][15] Again, because the disease is rarely seen in western countries, identification of the bacterium B. pseudomallei in cultures may not actually trigger alarm bells in physicians unfamiliar with the disease.[16] Routine biochemical methods for identification of bacteria vary widely in their identification of this organism: the API 20NE system accurately identifies B. pseudomallei in 99% of cases,[17] as does the automated Vitek 1 system, but the automated Vitek 2 system only identifies 19% of isolates.[15]
The pattern of resistance to antimicrobials is distinctive, and helps to differentiate the organism from P. aeruginosa. The majority of B. pseudomallei isolates are intrinsically resistant to all aminoglycosides (via an efflux pump mechanism),[18] but sensitive to co-amoxiclav:[19] this pattern of resistance almost never occurs in P. aeruginosa and is helpful in identification.[20]
Molecular methods (PCR) of diagnosis are possible, but not routinely available for clinical diagnosis.[21][22] Fluorescence in situ hybridisation has also been described, but has not been clinical validated and it not commercially available .[23] In Thailand, a latex agglutination assay is widely used.[17] A rapid immunofluorescence technique is also available in a small number of centres in Thailand.[24]
Disinfection
B. pseudomallei is susceptible to numerous disinfectants including benzalkonium chloride, iodine, mercuric chloride, potassium permanganate, 1% sodium hypochlorite, 70% ethanol, 2% glutaraldehyde and to a lesser extent, phenolic preparations.[25] B. pseudomallei is effectively killed by the commercial disinfectants, Perasafe and Virkon.[26] The microorganism can also be destroyed by heating to above 74°C for 10 min or by UV irradiation. B. pseudomallei is not reliably disinfected by chlorine.[27][28]
Medical importance
Main article: Melioidosis
B. pseudomallei infection in humans is called melioidosis. The mortality of melioidosis is 20 to 50% even with treatment.[19]
Antibiotic treatment and sensitivity testing
Main article: Melioidosis treatment
The antibiotic of choice is ceftazidime.[19] While various antibiotics are active in vitro (e.g., chloramphenicol, doxycycline, co-trimoxazole), they have been proven to be inferior in vivo for the treatment of acute melioidosis.[29] Disc diffusion tests are unreliable when looking for co-trimoxazole resistance in B. pseudomallei (they greatly overestimate resistance) and Etests or agar dilution tests should be used in preference.[30][31] The actions of co-trimoxazole and doxycycline are antagonistic, which suggests that these two drugs ought not to be used together.[32]
The organism is intrinsically resistant to gentamicin[33] and to colistin, and this fact is helpful in the identification of the organism.[34] Kanamycin is used to kill B. pseudomallei in the laboratory, but the concentrations used are much higher than those achievable in humans.[35]
Pathogenicity mechanisms and virulence factors
B. pseudomallei is an "accidental pathogen". It is an environmental organism that has no requirement to pass through an animal host in order to replicate. From the point of view of the bacterium, human infection is an evolutionary "dead end".[36]
Strains which cause disease in humans differ from those causing disease in other animals by possessing certain genomic islands.[37] It may have the ability to cause disease in humans because of DNA it has acquired from other microorganisms.[37] The mutation rate is also high, and the organism continues to evolve even after infecting the host.[38]
B. pseudomallei is able to invade cells (it is an intracellular pathogen).[39] It is able to polymerise actin and to spread from cell to cell, causing cell fusion and the formation of multinucleate giant cells.[40] The bacterium also expresses a toxin called lethal factor 1.[41] B. pseudomallei is one of the first proteobacteria to be identified as containing an active Type 6 secretion system. it is also the only organism identified that contains up to six different type 6 secretion systems.[42]
B. pseudomallei is intrinsically resistant to a large number of antimicrobial agents. One important mechanism is that it is able to pump drugs out of the cell, and this mediates resistance to aminoglycosides (AmrAB-OprA), tetracyclines, fluoroquinolones and macrolides (BpeAB-OprB).[43]
Vaccine candidates
There are no vaccine currently available, but a number of vaccines candidates have been suggested. Aspartate-β-semialdehyde dehydrogenase (asd) gene deletion mutants are auxotrophic for diaminopimelate (DAP) in rich medium and auxotrophic for DAP, lysine, methionine, and threonine in minimal medium.[44] The Δasd bacterium (bacterium with the asd gene removed) protects against inhalational melioidosis in mice.[45]
References
- ^ Yabuuchi, E; Kosako, Y; Oyaizu, H; Yano, I; Hotta, H; Hashimoto, Y; Ezaki, T; Arakawa, M (1992). "Proposal of Burkholderia gen. nov. and transfer of seven species of the genus Pseudomonas homology group II to the new genus, with the type species Burkholderia cepacia (Palleroni and Holmes 1981) comb. nov.". Microbiol Immunol 36 (12): 1251–1275. PMID 1283774.
- ^ "Burkholderia pseudomallei". VirginiaTech Pathogen Database. http://pathport.vbi.vt.edu/pathinfo/pathogens/Burkholderia_pseudomallei.html. Retrieved 2006-03-26.
- ^ Lee YH, Chen Y, Ouyang X, Gan YH (2010). "Identification of tomato plant as a novel host model for Burkholderia pseudomallei". BMC Microbiol 10: 28. doi:10.1186/1471-2180-10-28. PMC 2823722. PMID 20109238. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2823722/.
- ^ Haase A, Janzen J, Barrett S, Currie B (July 1997). "Toxin production by Burkholderia pseudomallei strains and correlation with severity of melioidosis". Journal of medical microbiology 46 (7): 557–63. doi:10.1099/00222615-46-7-557. PMID 9236739.
- ^ a b Peacock SJ, Chieng G, Cheng AC, et al. (October 2005). "Comparison of Ashdown's medium, Burkholderia cepacia medium, and Burkholderia pseudomallei selective agar for clinical isolation of Burkholderia pseudomallei". Journal of clinical microbiology 43 (10): 5359–61. doi:10.1128/JCM.43.10.5359-5361.2005. PMC 1248505. PMID 16208018. http://jcm.asm.org/cgi/pmidlookup?view=long&pmid=16208018.
- ^ Chaiyaroj SC, Kotrnon K, Koonpaew S, Anantagool N, White NJ, Sirisinha S (1999). "Differences in genomic macrorestriction patterns of arabinose-positive (Burkholderia thailandensis) and arabinose-negative Burkholderia pseudomallei". Microbiology and immunology 43 (7): 625–30. PMID 10529102.
- ^ a b Walsh AL, Wuthiekanun V (1996). "The laboratory diagnosis of melioidosis.". Br J Biomed Sci 53 (4): 249–53. PMID 9069100.
- ^ Brundage WG, Thuss CJ, Walden DC (March 1968). "Four fatal cases of melioidosis in U. S. soldiers in Vietnam. Bacteriologic and pathologic characteristics". The American journal of tropical medicine and hygiene 17 (2): 183–91. PMID 4869109. http://www.ajtmh.org/cgi/pmidlookup?view=long&pmid=4869109.
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- ^ Wattiau P, Van Hessche M, Neubauer H, Zachariah R, Wernery U, Imberechts H (March 2007). "Identification of Burkholderia pseudomallei and related bacteria by multiple-locus sequence typing-derived PCR and real-time PCR". Journal of clinical microbiology 45 (3): 1045–8. doi:10.1128/JCM.02350-06. PMC 1829090. PMID 17251403. http://jcm.asm.org/cgi/pmidlookup?view=long&pmid=17251403.
- ^ Hagen RM, Frickmann H, Elschner M, et al. (2011). "Rapid identification of Burkholderia pseudomallei and Burkholderia mallei by fluorescence in situ hybridization (FISH) from culture and paraffin-embedded tissue samples". Int J Med Microbiol 301 (7): 585–90. doi:10.1016/j.ijmm.2011.04.017. PMID 21658996.
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- ^ Miller, WR; Pannell, L; Cravitz, L; Tanner, WA; Ingalls, MS (1948). "Studies on certain biological characteristics of Malleomyces mallei and Malleomyces pseudomallei: I. Morphology, cultivation, viability, and isolation from contaminated specimens". J Bacteriol 55 (1): 115–126. PMC 518415. PMID 16561426. //www.ncbi.nlm.nih.gov/pmc/articles/PMC518415/.
- ^ Wuthiekanun V, Wongsuwan G, Pangmee S, Teerawattanasook N, Day NP, Peacock SJ (2010). "Perasafe, Virkon and bleach are bactericidal for Burkholderia pseudomallei, a select agent and the cause of melioidosis". J Hosp Infect 77 (2): 183–184. doi:10.1016/j.jhin.2010.06.026. PMC 3036794. PMID 20832143. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3036794/.
- ^ Howard K, Inglis TJJ (2003). "The effect of free chlorine on Burkholderia pseudomallei in potable water". Water Res 37 (18): 4425–4432. doi:10.1016/S0043-1354(03)00440-8.
- ^ Howard K, Inglis TJJ (2005). "Disinfection of Burkholderia pseudomallei in potable water". Water Res 39 (6): 1085–1092. doi:10.1016/j.watres.2004.12.028. PMID 15766962.
- ^ White NJ, Dance DA, Chaowagul W, Wattanagoon Y, Wuthiekanun V, Pitakwatchara N (September 1989). "Halving of mortality of severe melioidosis by ceftazidime". Lancet 2 (8665): 697–701. doi:10.1016/S0140-6736(89)90768-X. PMID 2570956. http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(89)90768-X.
- ^ Lumbiganon P, Tattawasatra U, Chetchotisakd P, et al. (2000). "Comparison between the antimicrobial susceptibility of Burkholderia pseudomallei to trimethoprim-sulfamethoxazole by standard disk diffusion method and by minimal inhibitory concentration determination". J Med Assoc Thai 83 (8): 856–60. PMID 10998837.
- ^ Wuthiekanun V, Cheng AC, Chierakul W, et al. (2005). "Trimethoprim/sulfamethoxazole resistance in clinical isolates of Burkholderia pseudomallei". J Antimicrob Chemother 55 (6): 1029–31. doi:10.1093/jac/dki151. PMID 15886263.
- ^ Saraya S, Soontornpas C, Chindavijak B, Mootsikapun P (2009). "In vitro interactions between cotrimoxazole and doxycycline in Burkholderia pseudomallei: how important is this combination in maintenance therapy of melioidosis?". Indian J Med Microbiol 27 (1): 88–9. PMID 19172079.
- ^ Trunck LA; Propst, KL; Wuthiekanun, V; Tuanyok, A; Beckstrom-Sternberg, SM; Beckstrom-Sternberg, JS; Peacock, SJ; Keim, P et al. (2009). Picardeau, Mathieu. ed. "Molecular basis of rare aminoglycoside susceptibility and pathogenesis of Burkholderia pseudomallei clinical isolates from Thailand". PLoS Negl Trop Dis 3 (9): e519. doi:10.1371/journal.pntd.0000519. PMC 2737630. PMID 19771149. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2737630/.
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- ^ Kespichayawattana W, Intachote P, Utaisincharoen P, Stitaya Sirisinha S (2004). "Virulent Burkholderia pseudomallei is more efficient than avirulent Burkholderia thailandensis in invasion of and adherence to cultured human epithelial cells". Microbial Pathogenesis 36 (5): 287–29. doi:10.1016/j.micpath.2004.01.001. PMID 15043863.
- ^ Nandi T, Ong C, Singh AP, Boddey J, Atkins T, Sarkar-Tyson M, Essex-Lopresti AE, Chua HH, Pearson T, Kreisberg JF, Nilsson C, Ariyaratne P, Ronning C, Losada L, Ruan Y, Sung WK, Woods D, Titball RW, Beacham I, Peak I, Keim P, Nierman WC, Tan P (2010). Guttman, David S.. ed. "A genomic survey of positive selection in Burkholderia pseudomallei provides insights into the evolution of accidental virulence". PLoS Pathog. 6 (4): e1000845. doi:10.1371/journal.ppat.1000845. PMC 2848565. PMID 20368977. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2848565/.
- ^ a b Sim SH, Yu Y, Lin CH, et al. (October 2008). Achtman, Mark. ed. "The core and accessory genomes of Burkholderia pseudomallei: implications for human melioidosis". PLoS Pathog. 4 (10): e1000178. doi:10.1371/journal.ppat.1000178. PMC 2564834. PMID 18927621. http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000178.
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- ^ Kespichayawattana W, Rattanachetkul S, Wanun T, et al. (2000). "Burkholderia pseudomallei induces cell fusion and actin-associated membrane protrusion: a possible mechanism for cell-to-cell spreading". Infect. Immun. 68 (9): 5377–84. doi:10.1128/IAI.68.9.5377-5384.2000. PMC 101801. PMID 10948167. //www.ncbi.nlm.nih.gov/pmc/articles/PMC101801/.
- ^ Cruz-Migoni A, Hautbergue GM, Artymiuk PJ, et al. (2011). "A Burkholderia pseudomallei toxin inhibits helicase activity of translation factor eIF4A.". Science 334 (6057): 821–4. doi:10.1126/science.1211915. PMID 22076380.
- ^ Shalom G, Shaw JG, Thomas MS (August 2007). "In vivo expression technology identifies a type VI secretion system locus in Burkholderia pseudomallei that is induced upon invasion of macrophages". Microbiology 153 (Pt 8): 2689–99. doi:10.1099/mic.0.2007/006585-0. PMID 17660433. http://mic.sgmjournals.org/cgi/pmidlookup?view=long&pmid=17660433.
- ^ Mima T, Schweizer HP (2010). "The BpeAB-OprB efflux pump of Burkholderia pseudomallei 1026b does not play a role in quorum sensing, virulence factor production or extrusion of aminoglycosides but is a broad-spectrum drug efflux system". Antimicrob. Agents Chemother. 54 (8): 3113–20. doi:10.1128/AAC.01803-09. PMC 2916348. PMID 20498323. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2916348/.
- ^ Norris MH, Kang Y, Lu D, Wilcox BA, Hoang TT (2009). "Glyphosate resistance as a novel select-agent-compliant, non-antibiotic-selectable marker in chromosomal mutagenesis of the essential genes asd and dapB of Burkholderia pseudomallei.". Appl Environ Microbiol 75: 6062–6075. doi:10.1128/AEM.00820-09.
- ^ Norris MH, Propst KL, Kang Y, et al. (2011). "The Burkholderia pseudomallei Δasd mutant exhibits attenuated intracellular infectivity and imparts protection against acute inhalation melioidosis in mice". Infect Immun 79 (10): 4010–8. doi:10.1128/IAI.05044-11. PMC 3187240. PMID 21807903. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3187240/.
External links
- Burkholderia pseudomallei genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID
- Getting a Grip on the Great Mimicker: Secrets of a Stealth Organism from the Wellcome Trust.
- Pathema Burkholderia resource
Infectious diseases · Bacterial diseases: Proteobacterial G− (primarily A00–A79, 001–041, 080–109)
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α |
Rickettsiales
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Rickettsiaceae/
(Rickettsioses)
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Typhus
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Rickettsia typhi (Murine typhus) · Rickettsia prowazekii (Epidemic typhus, Brill–Zinsser disease, Flying squirrel typhus)
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Spotted
fever
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Tick-borne
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Rickettsia rickettsii (Rocky Mountain spotted fever) · Rickettsia conorii (Boutonneuse fever) · Rickettsia japonica (Japanese spotted fever) · Rickettsia sibirica (North Asian tick typhus) · Rickettsia australis (Queensland tick typhus) · Rickettsia honei (Flinders Island spotted fever) · Rickettsia africae (African tick bite fever) · Rickettsia parkeri (American tick bite fever) · Rickettsia aeschlimannii (Rickettsia aeschlimannii infection)
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Mite-borne
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Rickettsia akari (Rickettsialpox) · Orientia tsutsugamushi (Scrub typhus)
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Ehrlichiosis: Anaplasma phagocytophilum (Human granulocytic anaplasmosis, Anaplasmosis) · Ehrlichia chaffeensis (Human monocytic ehrlichiosis) · Ehrlichia ewingii (Ehrlichiosis ewingii infection)
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Rhizobiales
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Brucellaceae
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Brucella abortus (Brucellosis)
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Bartonellaceae
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Bartonellosis: Bartonella henselae (Cat scratch disease) · Bartonella quintana (Trench fever) · either henselae or quintana (Bacillary angiomatosis) · Bartonella bacilliformis (Carrion's disease, Verruga peruana)
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β |
Neisseriales
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M+ Neisseria meningitidis/meningococcus (Meningococcal disease, Waterhouse-Friderichsen syndrome, Meningococcal septicaemia)
M- Neisseria gonorrhoeae/gonococcus (Gonorrhea)
ungrouped: Eikenella corrodens/Kingella kingae (HACEK) · Chromobacterium violaceum (Chromobacteriosis infection)
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Burkholderiales
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Burkholderia pseudomallei (Melioidosis) · Burkholderia mallei (Glanders) · Burkholderia cepacia complex · Bordetella pertussis/Bordetella parapertussis (Pertussis)
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γ |
Enterobacteriales
(OX-)
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Lac+
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Klebsiella pneumoniae (Rhinoscleroma, Klebsiella pneumonia) · Klebsiella granulomatis (Granuloma inguinale) · Klebsiella oxytoca
Escherichia coli: Enterotoxigenic · Enteroinvasive · Enterohemorrhagic · O157:H7 · O104:H4 (Hemolytic-uremic syndrome)
Enterobacter aerogenes/Enterobacter cloacae
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Slow/weak
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Serratia marcescens (Serratia infection) · Citrobacter koseri/Citrobacter freundii
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Lac-
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H2S+
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Salmonella enterica (Typhoid fever, Paratyphoid fever, Salmonellosis)
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H2S-
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Shigella dysenteriae/sonnei/flexneri/boydii (Shigellosis, Bacillary dysentery) · Proteus mirabilis/Proteus vulgaris · Yersinia pestis (Plague/Bubonic plague) · Yersinia enterocolitica · Yersinia pseudotuberculosis
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Pasteurellales
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Haemophilus: H. influenzae (Haemophilus meningitis, Brazilian purpuric fever) · H. ducreyi (Chancroid) H. parainfluenzae (HACEK)
Pasteurella multocida (Pasteurellosis) · Actinobacillus (Actinobacillosis)
Aggregatibacter actinomycetemcomitans (HACEK)
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Legionellales
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Legionella pneumophila/Legionella longbeachae (Legionellosis) · Coxiella burnetii (Q fever)
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Thiotrichales
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Francisella tularensis (Tularemia)
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Vibrionales
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Vibrio cholerae (Cholera) · Vibrio vulnificus · Vibrio parahaemolyticus · Vibrio alginolyticus · Plesiomonas shigelloides
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Pseudomonadales
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Pseudomonas aeruginosa (Pseudomonas infection) · Moraxella catarrhalis · Acinetobacter baumannii
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Xanthomonadales
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Stenotrophomonas maltophilia
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Cardiobacteriales
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Cardiobacterium hominis (HACEK)
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Aeromonadales
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Aeromonas hydrophila/Aeromonas veronii (Aeromonas infection)
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Campylobacterales
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Campylobacter jejuni (Campylobacteriosis, Guillain–Barré syndrome) · Helicobacter pylori (Peptic ulcer, MALT lymphoma) · Helicobacter cinaedi (Helicobacter cellulitis)
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gr+f/gr+a (t)/gr-p (c)/gr-o
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drug (J1p, w, n, m, vacc)
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